Recombinant Human CDKN3 protein

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

The protein CDKN3 also known as Cyclin-Dependent Kinase Inhibitor 3 functions primarily as a phosphatase. It removes phosphate groups from molecules specifically targeting the phosphorylated threonine and serine residues. This action regulates cell cycle progression enabling proper cell division. CDKN3 has a molecular mass of approximately 42 kDa. This protein expresses widely in human tissues with significant levels found in the liver lung and heart. Its regulation and expression are important for maintaining normal cellular functions.

Biological function summary

CDKN3 plays a fundamental role in cell cycle control. It forms complexes with various cyclin-dependent kinases (CDKs) particularly CDK1 and CDK2 inhibiting their activity. By controlling these CDKs CDKN3 ensures proper transition through cell cycle phases. This regulation prevents unplanned cell proliferation and maintains genomic integrity. CDKN3's interaction with CDKs highlights its importance in controlling cell growth and preventing the cell cycle's derailment.

Pathways

CDKN3's role significantly impacts the cell cycle and DNA damage response pathways. It influences the G1/S and G2/M checkpoints through its interaction with CDK1 and CDK2 forming an integral part of these critical pathways that control cell division timing. CDKN3 also extends its influence to other proteins like Cyclin A and Cyclin B impacting their function and stability during cell cycle regulation. These interactions underpin CDKN3's involvement in ensuring that cells only proceed to divide when conditions are optimal.

CDKN3 has been implicated in the development of various cancers including liver and bladder cancer. Alterations in CDKN3 expression or function can lead to unchecked cell division and tumor progression. In the context of these cancers CDKN3 often interacts with other proteins like CDC25A which further influences its role in cell proliferation. By understanding these disease-related interactions researchers can better target CDKN3 for therapeutic interventions aimed at restoring normal cell cycle control in cancerous tissues.